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Intersecting Vulnerabilities

  • Writer: Emma Rice
    Emma Rice
  • 3 days ago
  • 3 min read

Previous research has shown that depression is associated with an increased risk of AD. At the same time, studies indicate that Black individuals are disproportionately affected by AD and related dementias compared to white individuals. So how might race, depression, and Alzheimer’s Disease (AD) be related? In a recent study conducted by Kamal and colleagues at McGill University in Canada, they looked at white matter hypointensities (WMHs) to investigate this question. The term “white matter hypointensity” refers to a feature seen on MRI scans of the brain. When looking at an MRI of the brain, different parts of the brain show up in different shades of gray. The brain’s “white matter” contains bundles of nerve axons along which signals travel to act on other neurons. Sometimes spots within the white matter stand out from the surrounding area. These are the areas we call white matter hypointensities. These WMHs are known to be associated with cognitive decline and dementia (Dadar 2019). In the study, Kamal and colleagues used this knowledge and the evidence that depression is also associated with cognitive decline to look at the differences that occur with race.


Data for the study was sourced from the National Alzheimer’s Coordinating Center (NACC) database and consisted of 2411 participants: 2133 white adults and 278 Black adults. By analyzing the WMH burden and rates of depression among both groups, they were able to determine that for Black older adults, the presence of depression was associated with greater WMH burden, a relationship that was not present among the white older adults. Additionally, they found that the WMH burden experienced by Black older adults had a greater effect on cognition, such that they performed worse on memory and thinking tests. Overall, these findings suggest that depression may be a greater risk factor for cognitive decline in Black individuals than white individuals, a finding that is important because it can not only influence how doctors approach their patients’ care, but also further emphasizes the importance of racial representation within AD research.


In addition, Kamal and colleagues also found that Black adults had a greater overall WMH burden than their white counterparts, in line with existing research on the topic. This was true even after accounting for the greater vascular risk factors, also known to increase the risk of dementia, experienced by Black individuals compared to white individuals. Several factors may contribute to this disparity, including the inflammatory effects of chronic stress linked to systemic racism and social inequities experienced by the Black community. While more research is needed to clarify how depression influences Alzheimer’s disease risk, this study underscores the urgent need to increase the inclusion of Black individuals in AD research. Our research team at UCSD partners with UCLA on the Black Women: Inflammation and Tau Study (BWITS), a study dedicated to advancing brain health research specifically for Black/African American women. While Black women face a higher risk of Alzheimer’s disease, they remain underrepresented in research. BWITS aims to change this discrepancy by exploring how factors like inflammation, insulin resistance, physical activity, and social determinants of health may influence memory, thinking, and tau protein changes over time.


We are currently enrolling Black women aged 60 and older. Participants complete 3 study visits over 2 years, all conducted in community settings. By joining BWITS, you can contribute to research that centers Black women’s health and helps shape more equitable approaches to Alzheimer’s prevention and care.


To learn more, visit www.b-wits.org or contact our team at study@b-wits.org.


Article of Interest:

Kamal F, Moqadam R, Morrison C, Dadar M. Intersecting vulnerabilities: race, depression, and white matter hypointensity burden in aging. Alzheimers Dement (Amst). 2026;18(1):e70252. Published 2026 Feb 9. doi:10.1002/dad2.70252

 
 
 

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